Analgesic and opioid involvement in the shock-elicited activity and escape deficits produced by inescapable shock

Three experiments examined the involvement of analgesic processes and endogenous opioids in the production of the shuttlebox escape acquisition and unconditioned activity deficits which follow exposure to inescapable shock. Experiment 1 found that the opiate antagonist naltrexone administered before the inescapable shock session interfered with the shuttlebox escape acquisition deficit which would normally follow. Experiment 2 found naltrexone to completely prevent the unconditioned activity deficit. The final experiment revealed that dexamethasone, a synthetic glucocorticoid which abolishes the analgesia produced by inescapable shock, reversed the activity deficit. These results indicate that endogenous opioids may be involved in the production of both the escape acquisition and activity deficits. They also suggest that the analgesia produced by these opioids may participate in the mediation of the activity deficit, even though analgesia is not involved in producing the shuttlebox acquisition deficit.